Some of bicyclic amino derivatives of the present invention have known to be useful as thromboxane A.sub.2 (TXA.sub.2) antagonists (Japanese Patent Publication (KOKOKU) No. 79060/1993). However, the Japanese Patent Publication (KOKOKU) No. 79060/1993 only describes that the compounds are useful as TXA.sub.2 antagonist, and does not suggest the usefulness thereof as PGD.sub.2 antagonist as disclosed by the present invention.
Namely, the TXA.sub.2 is known to have activities such as action against platelet agglutination, thrombogenesis, etc. The TXA.sub.2 antagonist has therefore been considered to be useful as anti-thrombotic agent, and also in the treatment of myocardial infarction or asthma by antagonizing against TXA.sub.2.
On the other hand, the PGD.sub.2 antagonist of the present invention is useful in the improvement of conditions due to excessive production of PGD.sub.2. Specifically, it is useful as a drug for treating diseases in which mast cell dysfunction is involved, for example, systemic mastocytosis and disorder of systemic mast cell activation, and also tracheal contraction, asthma, allergic rhinitis, allergic conjunctivitis, urticaria, injury due to ischemic reperfusion, and inflammation.
As is apparent from the above, the TXA.sub.2 antagonist and the PGD.sub.2 antagonist are completely different from each other in terms of the active site, mechanism of action, and application, and have quite different characteristics. Accordingly, it has never been expected that any compound could possess these activities simultaneously.
PGD.sub.2 is produced through PGG.sub.2 and PGH.sub.2 from arachidonic acid by the action of cyclooxygenase activated by immunological or unimmunological stimulation and is the major prostanoid that is produced and released from mast cells. PGD.sub.2 has various potent physiological and pathological activities. For example, PGD.sub.2 can cause strong tracheal contraction, which leads to bronchial asthma, and, in a systemic allergic state, it can dilate the peripheral vessels, which leads to an anaphylactic shock. Especially, much attention has been paid on the idea that PGD.sub.2 is one of the causal substances responsible to the onset of nasal occlusion in the allergic rhinitis. Therefore, it has been proposed to develop an inhibitor against the biosynthesis of PGD.sub.2 or an antagonist of PGD.sub.2 receptor as a drug for the reduction of nasal occlusion. However, the inhibitor of PGD.sub.2 biosynthesis possibly affects greatly the synthesis of prostaglandins in other organisms, and therefore, it is desirable to develop an antagonist (blocker) specific to PGD.sub.2 receptor.